Co-treatment of mouse antral follicles with 17β-estradiol interferes with mono-2-ethylhexyl phthalate (MEHP)-induced atresia and altered apoptosis gene expression

Zelieann R Craig, Jeffrey Singh, Rupesh K. Gupta, Jodi A. Flaws

Research output: Contribution to journalArticle

15 Citations (Scopus)

Abstract

Mono-2-ethyhexyl phthalate (MEHP) is a metabolite of a plasticizer found in many consumer products. MEHP inhibits mouse ovarian follicle growth by reducing 17β-estradiol (E2) production. Yet, whether MEHP causes follicle death (atresia) is unclear. We hypothesized that MEHP causes atresia by altering apoptosis gene expression, and that E2 co-treatment blocks these effects. Follicles were exposed to MEHP (0.36-36μM)±E2 for 48-96h to determine the effect of MEHP±E2 on atresia and gene expression. MEHP increased atresia, but this effect was blocked by co-treatment with E2. MEHP increased the expression of the pro-apoptotic gene Aifm1, but decreased that of the pro-apoptotic gene Bok and the anti-apoptotic gene Bcl2l10. E2 interfered with MEHP-induced changes in Aifm1 and Bcl2l10. Our findings suggest that decreased E2 levels are required for MEHP-induced follicle atresia and that Aifm1, Bok, and Bcl2l10 are involved in this process.

Original languageEnglish (US)
Pages (from-to)45-51
Number of pages7
JournalReproductive Toxicology
Volume45
DOIs
StatePublished - Jun 2014
Externally publishedYes

Fingerprint

Gene expression
Estradiol
Apoptosis
Gene Expression
Genes
Plasticizers
Ovarian Follicle
Consumer products
mono-(2-ethylhexyl)phthalate
Antral
Metabolites
Cause of Death
Growth

Keywords

  • Apoptosis
  • Estradiol
  • Follicle
  • Ovary
  • Phthalate

ASJC Scopus subject areas

  • Toxicology
  • Medicine(all)

Cite this

Co-treatment of mouse antral follicles with 17β-estradiol interferes with mono-2-ethylhexyl phthalate (MEHP)-induced atresia and altered apoptosis gene expression. / Craig, Zelieann R; Singh, Jeffrey; Gupta, Rupesh K.; Flaws, Jodi A.

In: Reproductive Toxicology, Vol. 45, 06.2014, p. 45-51.

Research output: Contribution to journalArticle

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